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[FONT=&quot]IGF 1 lr3 as we know is a fantastic growth factor for bodybuilders and athletes of all kinds. Used for Building quality lean muscle mass, as well as for its ability to keep you lean by way of signa;ling the body to burn fat for energy. We have also read and posted many studies here at MuscleChemistry regarding Insulin-like growth factor 1 healing power and regenerative capabilities on tendons and cartlidge and it promotes collagen synthesis as well. But lately I have been reading a ton on IGF 1 treatment for Central Nervous System Disorders.

So Enjoy:

The therapeutic potential of IGF-1 was found to be relevant to the treatment of several CNS disorders, most notably Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer’s Disease, Parkinson’s Disease, and autism spectrum disorder. Table 1 categorizes the human clinical trials in specific CNS diseases.
[h=3]Table 1[/h]Clinical Trials with IGF-1 in CNS DisordersOverview of clinical trials using IGF-1 as a therapeutic agent in CNS disorders to date

[TABLE="class: rendered small default_table"]
<thead style="border: none;">[TR]
[TH="bgcolor: inherit, colspan: 1, align: center"][/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Intervention[/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Author
and Year[/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Sample
Size[/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Study
Design[/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Duration
of
Treatment[/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Primary
Outcome
Measure[/TH]
[TH="bgcolor: inherit, colspan: 1, align: center"]Outcome[/TH]
[/TR]
</thead><tbody style="border-top: 1px solid rgb(136, 136, 136);">[TR]
[TD="colspan: 1, align: center"]Multiple
Sclerosis[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](J. A. Frank et al., 2002)[/TD]
[TD="colspan: 1, align: center"]7[/TD]
[TD="colspan: 1, align: center"]Open-label
crossover[/TD]
[TD="colspan: 1, align: center"]6 months[/TD]
[TD="colspan: 1, align: center"]Contrast
enhancing lesion
frequency on
MRI[/TD]
[TD="colspan: 1, align: center"]Negative[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Amyotrophic
Lateral
Sclerosis[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](Nagano, Shiote, et al., 2005)[/TD]
[TD="colspan: 1, align: center"]9[/TD]
[TD="colspan: 1, align: center"]Double-
blind,
randomized
clinical[/TD]
[TD="colspan: 1, align: center"]9 months[/TD]
[TD="colspan: 1, align: center"]Norris Scales[/TD]
[TD="colspan: 1, align: center"]Positive[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Amyotrophic
Lateral
Sclerosis[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](Lai et al., 1997)[/TD]
[TD="colspan: 1, align: center"]141[/TD]
[TD="colspan: 1, align: center"]Double
blind,
placebo
controlled,
parallel
group[/TD]
[TD="colspan: 1, align: center"]9 months[/TD]
[TD="colspan: 1, align: center"]Appel
Amyotrophic
Lateral Sclerosis
rating scale[/TD]
[TD="colspan: 1, align: center"]Positive[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Amyotrophic
Lateral
Sclerosis[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](Borasio et al., 1998)[/TD]
[TD="colspan: 1, align: center"]183[/TD]
[TD="colspan: 1, align: center"]Double
blind,
placebo
controlled,
parallel
group[/TD]
[TD="colspan: 1, align: center"]9 months[/TD]
[TD="colspan: 1, align: center"]Appel
Amyotrophic
Lateral Sclerosis
rating scale[/TD]
[TD="colspan: 1, align: center"]Negative[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Amyotrophic
Lateral
Sclerosis[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](Sorenson et al., 2008)[/TD]
[TD="colspan: 1, align: center"]330[/TD]
[TD="colspan: 1, align: center"]Double
blind,
placebo
controlled,
parallel
group[/TD]
[TD="colspan: 1, align: center"]2 years[/TD]
[TD="colspan: 1, align: center"]Rate of change
in the averaged
manual muscle
testing score
(MMT)[/TD]
[TD="colspan: 1, align: center"]Negative[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Alzheimer’s
Dementia[/TD]
[TD="colspan: 1, align: center"]MK-677[/TD]
[TD="colspan: 1, align: center"](Sevigny et al., 2008)[/TD]
[TD="colspan: 1, align: center"]563[/TD]
[TD="colspan: 1, align: center"]Double
blind,
placebo
controlled,
parallel
group[/TD]
[TD="colspan: 1, align: center"]12 months[/TD]
[TD="colspan: 1, align: center"]Clinician’s
Interview Based
Impression of
Change with
caregiver input
(CIBIC-plus)[/TD]
[TD="colspan: 1, align: center"]Negative[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Phelan-
McDermid
syndrome[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](Kolevzon et al., 2014)[/TD]
[TD="colspan: 1, align: center"]9[/TD]
[TD="colspan: 1, align: center"]Double
blind,
placebo
controlled,
crossover[/TD]
[TD="colspan: 1, align: center"]3 months[/TD]
[TD="colspan: 1, align: center"]Aberrant
Behavior
Checklist-Social
Withdrawal
subscale[/TD]
[TD="colspan: 1, align: center"]Positive[/TD]
[/TR]
[TR]
[TD="colspan: 1, align: center"]Rett
syndrome[/TD]
[TD="colspan: 1, align: center"]rhIGF-1[/TD]
[TD="colspan: 1, align: center"](Khwaja et al., 2014)[/TD]
[TD="colspan: 1, align: center"]9
(MAD)
12
(OLE)[/TD]
[TD="colspan: 1, align: center"]Unblind
multiple
ascending
dose and
open label
extension[/TD]
[TD="colspan: 1, align: center"]4 week
MAD
20 week
OLE[/TD]
[TD="colspan: 1, align: center"]Multiple
Cardiorespiratory
measures[/TD]
[TD="colspan: 1, align: center"]Positive[/TD]
[/TR]
</tbody>[/TABLE]

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Abbreviations: MK-677 = ibutamoren mesylate; MAD = multiple ascending dose; OLE = open-label extension






The extensive investigation of the effect of IGF-1 during development and the continued discovery of its diverse roles throughout the CNS exemplifies the presence of common underlying pathways responsible for neuronal development. Although many different genetic mutations and disrupted pathways lead to syndromes associated with ASD, there is significant overlap in their molecular and electrophysiological deficits. Specific deficits in synaptic function and plasticity in glutamate signaling have been consistently documented in various forms of ASD using mouse and human neuronal models and have been rescued with IGF-1. The link between synapse dysfunction and ASD suggest that treatment with IGF-1 may also have implications for ASD associated with disruptions in common underlying pathways. Preliminary studies in children with PMS and Rett syndrome have been successful, and IGF-1 may also be a promising therapeutic candidate in other single gene causes of ASD and perhaps in idiopathic ASD; a trial is underway with IGF-1 in ASD defined broadly (ClinicalTrials.gov Identifier: NCT01970345). Although definitive studies are needed, pilot data suggest the promise of IGF-1 in neurodevelopmental disorders associated with ASD.
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[FONT=&quot]​[h=3]Highlights[/h]

  • IGF-1 is necessary for proper development of the central nervous system
  • IGF-1 dysregulation leads to neuronal dysfunction and severe developmental disorders
  • IGF-1 may be a safe and potentially effective treatment for several CNS disorders


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